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2.
04250065 Psychology of Pain
What is Phantom Limp Pain?
Phantom limb pain (PLP) is a phenomenon referring to the pain experienced from limb
that has previously been amputated or severed. PLP has a surprisingly high level of
prevalence, as it effects up to 72% of all amputees (Jensen et al, 1984 (1)
). They also found
that pain persisted until 7 years after amputation; Sherman et al (1980) (2)
found that no
more than 15% find total pain relief. Pain can be either episodic or continuous and is often
described as a ‘cramping, crushing or stabbing pain’ in the missing limb (Clement and Taunton,
2001 (3)
). Livingston (1943) (4)
suggested that a common feature is that the reported pain is
felt in definite parts of the phantom limb (e.g. the phantom hand is clenched so it feels
tired and painful).
What Causes Phantom Limb Pain?
A vast body of research has been conducted to determine the causes of this
phenomenon. It is widely accepted that it is a result of damage to the nerve endings in the
residual limb (A)
sending pain signals to the brain making it think that the limb is still there (5).
Sussman (1995) (6)
suggested that it starts in the homunculus (B)
, an area of the sensory
cortex (C)
. When a part of the actual body is lost, the corresponding part of the homunculus
remains, but is unable to handle the loss of information from the missing area. To remedy
this, the brain rewires its circuits so that the neighbouring neurons in the cortex invade the
vacant territory in order to compensate this loss of sensations; this is known as cortical
reorganisation.
Pharmacological Treatments of Phantom Limb Pain.
It is currently unsure whether there exists a stand-alone treatment for PLP. Although
there are many treatments that successfully help with aspects of PLP, there does not
appear to be a single treatment to eliminate phantom pain altogether. It appears as though
the best way to treat PLP is to employ a combination of pharmacological treatments with
psychological treatments.
Initially, measures are taken in an attempt to try and prevent the onset of PLP.
Calcitonin (D)
is a hormone produced by the thyroid gland (E)
to slow the rate at which the
body breaks down bone and is often used to prevent bone deterioration in the treatment of
postmenopausal osteoporosis (F)
. This is often administered intravenously (G)
during the week
following amputation (7)
.
Flor et al (2000) (8)
suggested that pharmacological treatments resulting in vasodilation
(H)
of the residual limb, ease burning PLP but not other features. Cramping phantom pain is
caused by muscle tension in the residual limb; clonazepam may relieve cramping PLP as it
depresses activity in the central nervous system and is used as a treatment of muscle
tension. Baclofen is also a muscle relaxant, often used to treat muscle spasms and
neuropathic (I)
pain syndromes, of which PLP is one. Although these treatments have proven
successful, they do not always eliminate phantom pain for all patients.

3.
04250065 Psychology of Pain
In cases where pain is severe, an opioid (J)
, such as morphine (K)
may be administered in
order to ease the pain. Sawynok (2003) (9)
suggests that Opioids are generally safe
treatments when closely monitored by health professionals. Although proven to be highly
successful in the treatment of severe pain, morphine is not without its dangers. If patients
are over – dosed, side effects such as sweating (in extreme cases causing hypothermia),
salivation and certain lung secretions which may depress lung function to the point of
respiratory arrest (L)
. Morphine is also known for causing both constipation and vomiting.
Research in this area suggests that although pharmacological treatments specialise in
easing certain types of PLP, they are not broad enough to cover all types of pain that are
experienced here. In order to account for this it is often useful to implement the use of
psychological treatments, to be used in conjunction with pharmacological treatments.
Psychological Treatments of Phantom Limb Pain.
Stress has been identified as a common factor in phantom limb pain. Arena et al (1990)
(10)
tested for relationships between situational stress and PLP in 27 male, 71 year old
amputees and found that 74% demonstrated significant stress - pain relationships. This
finding brings light to the possibility that psychological treatments may also be useful in the
alleviation of phantom pain.
There has been research into the effects of hypnosis as a treatment of PLP; Wain
(1986) (11)
suggested that hypnosis allows effective strategies to be implemented in order to
allow patients to gain control over their experienced pain. Although hypnosis has a good
reputation for having no pharmacological side effects, there is a debate about whether or
not all people are susceptible to hypnosis, Horn and Munafo (1997) (12)
suggests that people
react to hypnosis in many different ways, dependent upon their ‘hypnotisability’ which can
either facilitate or inhibit their openness to hypnotic suggestions. This may significantly
decrease its effectiveness. However, hypnosis is also regarded as a recognised relaxation
technique; this provides a basis for the assumption that relaxation may be a feasible
treatment for PLP.
Conclusion.
In conclusion, although there is much research to provide support for the use of
pharmacological treatments to eradicate PLP, most research points to specific drugs as an
appropriate treatment for certain aspects of the pain experienced in a phantom limb. At
present research has produced inconclusive findings for a stand – alone pharmacological
treatment for phantom limb pain. From, this it may be important to suggest a systematic
collaboration of pharmacological treatments such as a strictly monitored course of opioid
treatments to ease pain, with muscle relaxants to ease muscles cramping and a psychological
treatment such as hypnosis to promote relaxation. This collaboration of treatments may
need extensive research before being implemented as most pharmacological treatments
have unique side effects relating to each one, care must be made to ensure that these side
effects do not outweigh the initial pain.

4.
04250065 Psychology of Pain
Additional Resources.
Above is a diagram showing the Homunculus, which is a map of the body, within
the sensory cortex in the brain. Here the areas of the body that detect more
sensory information are represented much larger than areas which detect less
sensory information.

5.
04250065 Psychology of Pain
Glossary of Terms (13)
.
A. Residual Limb: - part of the amputated limb that is left behind (stump).
B. Homunculus (little man): - The nerve map of the human body that exists on
the parietal lobe of the human brain whereby each of its body parts is linked
with its corresponding area of the actual body.
C. Sensory Cortex: - located posterior to the central sulcus in the parietal
lobe receives sensory input from receptors in the body.
D. Calcitonin: - a hormone produced by the thyroid gland (E)
to slow the rate at
which the body breaks down bone.
E. Thyroid Gland: - located around the trachea, the thyroid gland is a gland
that makes and stores hormones which regulate heart rate, blood pressure
and body temperature.
F. Osteoporosis: - a chronic, progressive condition associated with
deterioration of bone tissue resulting in low bone mass.
G. Intravenous: - administration of medication directly into the vein.
H. Vasodilation: - Widening of the interior of the blood vessels as a result of
the relaxation of the muscular wall of the vessels.
I. Neuropathic: - pain which comes from injury to the nerves themselves and
not from injured body parts
J. Opioid: - A synthetic narcotic, resembling the naturally occurring opiates.
K. Morphine: - kills pain at low doses and makes you feel tranquil, increasing
your tolerance to pain. With morphine, the perception of pain is still there,
but the appreciation of the pain decreases
L. Respiratory arrest: - spontaneous respiration dude to damage caused to
the respiratory centre.
References.
• (1) Jensen TS, Krebs B, Nielsen J, Rasmussen P. Non-painful phantom limb
phenomena in amputees: incidence, clinical characteristics and temporal
course. Acta Neurol Scand 1984; 70: 407–14